Expression of macrophage CD14 receptor in the course of experimental inflammatory responses induced by lipopolysaccharide and muramyl dipeptide

نویسندگان

  • Z. Sladek
  • D. Rysanek
چکیده

The aim of this study was to determine whether expression of CD14 on macrophages is regulated differently during initiation and resolution of the inflammatory response caused by CD14-dependent (lipopolysaccharide) and CD14-independent (muramyldipeptide) bacterial signals. In cell suspensions from the site of inflammation we observed two types of macrophages: non-vacuolized (NMAC) and vacuolized (VMAC) cells. NMAC (monocyte-like cells) were dominant during the early stage of the inflammatory response, whilst VMAC contained phagocytosed apoptotic neutrophils in various stages of digestion. These latter cells were dominant during resolution (particularly at the last time point of 168 h). Intramammary instillation of muramyldipeptide (MDP) and lipopolysaccharide (LPS) resulted in a significant increase in the total count of CD14+ NMAC after 24 h (muramyldipeptide P < 0.01 and lipopolysaccharide P < 0.05) compared to phosphate buffered saline (PBS). During resolution of the inflammatory response, a gradual decrease in the total count of CD14+ NMAC was observed. The difference compared with PBS was significant at 48 h and 72 h after instillation of both bacterial agents (muramyldipeptide: P < 0.05; lipopolysaccharide: P < 0.05). A lower total count of CD14+ VMAC was observed as an effect of MDP and LPS at 24 h after induction (P < 0.05), when compared to PBS. During resolution, the total count of CD14+ VMAC increased. Differences (P < 0.01) were observed at 72 h and 168 h after LPS compared to PBS. We therefore assume that the expression of CD14 on macrophages is not regulated differently during the inflammatory responses caused by CD14-dependent and CD14-independent bacterial signals. On the other hand, the stage of the inflammatory response to MDP and LPS played an important role in the regulation of CD14 expression on macrophages.

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تاریخ انتشار 2008